Clin pharm - GN

Presentations of GN
- Nephrotic syndrome
o Cardinal features
proteinuria >3.5 g
oedema
hypoalbuminuria
o 2ndary thrombosis, hypercholesterolaemia, infections
(if recurrent, offer prophylaxis)
o Not usually associated with renal failure (if failing
consider overhydration, renal vein thrombosis image
with USS)
- Nephritic syndrome
o Cardinal features
Renal failure
Haematuria (with abnormal red cells on
microscopy acanthocytes, red cell casts)
Hypertension
Syndromes of GN
- Minimal change disease
o Only pathology to cause pure nephrotic syndrome
o Light microscopy: normal
o Immunofluorescence: normal
o EM: podocyte effacement
o Rx: steroids
- Membranous
o Basically nephrotic, but may have 1+ blood
o Light microscopy: nothing other than BM thickening
o Immunofluorescence:
o EM: BM thickening with subendothelial/subepithelial
dense deposits and spikes
o Associations: HBV, EBV, haematological malignancies,
lung and colon ca., drugs (gold, penicillamine main
differential for nephrotic in RA is AA amyloidosis causing
FSGS)
o Rx: steroids (although often resistant, and commonly
becomes chronic)
- FSGS
o Basically nephrotic, but may have 1+ blood
o Not a Dx consider DM and amyloidosis (AL/AA) as
causes
o Kimmelstiel-Wilson nodules (amorphous blob of
proteinaceous material) = DM
o Apple green fluorescence on Congo red stain =
amyloidosis

Membranoproliferative
o Nephritic syndrome with high protein leak (approaching
nephrotic levels)
o Causes acute severe renal failure
o Associations: HCV, cryoglobulinaemia, partial
lipodystrophy
IE: nephritic1; look for peripheral stigmata; signs occur at
height of infection
Post-infectious: nephritic; do an ASOT; occurs a few weeks
after infection
IgA: nephritic; commonest worldwide, often incidental finding
a few days after infection; if renal function deteriorates, a
renal biopsy is indicated (often triggered by infection)
Goodpastures nephritic; pulmonary-renal syndrome
Vasculitis: nephritic
o GPA: pulmonary-renal syndrome with nasal Sx; +ve
cANCA vs proteinase-3
o MPA: vasculitic rash and renal impairment; +ve pANCA
o Churg-Strauss (asthma, eosinophilia, vasculitis; +ve
pANCA vs. myeloperoxidase; can be triggered by LTRAs)
SLE: can do anything

Pathological patterns
- Focal segmental: only some of some glomeruli are affected
- Diffuse segmental: only some of all glomeruli are affected
- Focal global: all of some glomeruli are affected
- Diffuse global: all of all glomeruli are affected
- Sclerosis: scarring without inflammation (thickening within the
glomeruli without influx of inflammatory cells)
- Glomerulonephritis: inflammation present

1 Commonly associated with crescentic GN, deposition visible on

immunofluorescence (if IgA only = IgAN); granular staining is
present on immunofluorescence in type III conditions (due to distal
antibody formation, e.g. IgAN, post-infectious) cf. Goodpastures,
where there is linear deposition of IgG directly targeting the BM